在血管损伤后,Apolipoprotein J/clusterin在血管光滑肌细胞中被诱导
1First Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Kagoshima, Japan.
Circulation
|September 19, 2001
概括
在血管损伤后,Apolipoprotein J (apoJ) 显著上调,促进光滑肌肉细胞的增殖和迁移. 这表明apoJ在血管造形术后的静脉缩中起着关键作用.
科学领域:
- 分子生物学分子生物学
- 心血管研究研究心血管研究
- 基因表达分析 基因表达分析
背景情况:
- 皮肤透光冠状动脉血管整形术 (PTCA) 后的血管缩需要了解有效治疗的分子机制.
- 鉴定参与血管缩的基因对于开发新的治疗策略至关重要.
研究的目的:
- 为了识别与血管复原症发展有关的基因.
- 调查阿波利波蛋白J (apoJ) /集群蛋白在血管损伤反应中的作用.
主要方法:
- 在受气球伤害的子主动脉模型上使用差异化杂交.
- 北方斑块,西部斑块,免疫组织化学和现场杂交用于分析基因和蛋白质表达.
- 进行了子光滑肌细胞 (SMC) 的稳定传染,以研究apoJ功能.
主要成果:
- 在受伤后,六个cDNA克隆被上调,五个基因被构成性表达和上调.
- 在气球受伤后,Apolipoprotein J (apoJ) mRNA和蛋白质表达显著诱导,分别在24小时和2-8周达到峰值.
- ApoJ的表达局部化到介质和内膜中的平滑肌细胞,其表达刺激了SMC的增殖和迁移.
结论:
- 在血管损伤后,Apolipoprotein J (apoJ) 在介质和neointima中被显著诱导.
- 这些发现表明,apoJ在血管塑性手术后对静止病的发病有显著的贡献.
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